Abstract
Multiple sclerosis (MS) is a chronic inflammatory, demyelinating and neurodegenerative disorder. Since acetylcholine (ACh) is known to participate in the inflammatory response, we investigated the possible relationship between pro-inflammatory cytokines and acetylcholine levels in relapsing-remitting multiple sclerosis (RR-MS) patients. Levels of ACh and pro-inflammatory cytokines IL1-β and IL-17 were measured both in cerebrospinal fluid (CSF) and sera of 22 RR-MS patients in the relapsing phase and in 17 control subjects affected by other non-neurological diseases (OND). We observed higher levels of pro-inflammatory cytokines such as IL-1β and IL-17 in both CSF and serum of RR-MS patients compared to control subjects. Moreover, ACh levels were lower in CSF and serum of RR-MS patients compared to levels of control subjects. Although the relationship between high inflammatory cytokine levels and low ACh levels need to be further investigated in the future, our data suggest that IL-1β, and cytokines induced by it, such as IL-17 and ACh, may be involved in the pathogenesis of MS.
Highlights
Multiple sclerosis (MS) is characterized by an altered balance of pro- and anti-inflammatory cytokines that causes a high inflammatory state in the central nervous system (CNS), followed by selective destruction of myelin
IL-17 levels in serum were significantly elevated compared to control subjects (p < 0.05), while in the cerebrospinal fluid (CSF) the levels were lower than in the control group the differences were not statistically significant (p = 0.201). In both relapsing-remitting multiple sclerosis (RR-MS) and control group, the mean level of IL-17 was higher in the CSF than in serum (Table 1)
We measured the levels of IL-10, TNF-α and IL-4 both in CSF and sera and we did not find statistical differences between RR-MS patients and control subjects
Summary
Multiple sclerosis (MS) is characterized by an altered balance of pro- and anti-inflammatory cytokines that causes a high inflammatory state in the central nervous system (CNS), followed by selective destruction of myelin. IL-17 is one of the inflammatory cytokines secreted mainly by activated T cells and to TNF-α and IL-1, IL-17 has pro-inflammatory properties, playing a key role in the pathogenic mechanisms of MS [3]. Novel research tools and therapeutic approaches are oriented towards the identification of new molecules that may decrease the level of the noxious agents, and at the same time stimulate oligodendrocyte (OL) progenitors to proliferate and differentiate. It has been demonstrated that ACh reduces the inflammatory state as indicated by chronic administration of selective acetylcholinesterase inhibitors (AChEI) in autoimmune encephalomyelitis (EAE) animal models [4]. The muscarinic agonists are able to induce oligodendrocyte progenitor cell (OPC)
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